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PubMed2006

Herbicidal effects of statin pharmaceuticals in Lemna gibba.

Statin pharmaceuticals, heavily prescribed in the treatment of hypercholesterolemia, are competitive inhibitors of 3-hydroxy-3-methylglutaryl coenzyme-A reductase (HMGR). In plants, these compounds also inhibit HMGR, which regulates cytosolic isoprenoid biosynthesis in the mevalonic acid (MVA) pathway. Phytotoxicity was evaluated in the higher aquatic plant Lemna gibba exposed to atorvastatin and lovastatin for 7-days by measuring the concentrations of sterols and ubiquinone; products downstream in the MVA pathway. The efficiency of the parallel and unaffected methylerythritol phosphate pathway (MEP) was also evaluated by measuring the end product, plastoquinone. Statin treatment caused an accumulation of plastoquinone, and unexpectedly, ubiquinone, an artifact likely due to metabolite sharing from the plastidial MEP pathway. Statins were, however, highly phytotoxic to L. gibba and HPLC-UV analysis of plant extracts showed significantly decreased concentrations of both stigmasterol and beta-sitosterol, which are critical components of plant membranes and regulate morphogenesis and development. EC10 values for atorvastatin and lovastatin were as small as 26.1 and 32.8 microg/L, respectively. However, hazard quotients indicated that statins present little risk to the model higher aquatic plant Lemna gibba at environmentally relevant concentrations, even though pathway-specific endpoints were 2-3 times more sensitive than traditional gross morphological endpoints typically used in risk assessment.

Atorvastatin↗
PubMed1995

Changes in protein prenylation and prenyltransferase activity in the rat seminiferous epithelium during early stages of spermatogenesis.

Changes in protein prenyltransferase activity, levels of prenylated protein, and the type of isoprenoid modification was described in cells of rat seminifereous epithelium and correlated with differentiative events of spermatogenesis. The activity of protein farnesyltransferase (PFT) was at least 10-fold higher than that for protein geranylgeranyltransferase-I (PGGT-I) in seminiferous epithelium and spermatogenic cells of prepubertal rats of different ages. Both activities increased during the meiotic stages of differentiation and peaked at 23 days of age. The activity of farnesyltransferase in seminiferous epithelium was the same as that in mixed spermatogenic cell populations from animals aged 9 and 23 days, indicating that the activity of this enzyme in somatic cells and germ cells was similar at these ages. Farnesyltransferase activities were similar and low in both pachytene spermatocytes and round spermatids from adult rats; however, the activity in pachytene spermatocytes from 23-day old animals was 2-fold higher than in adults. The highest activity was associated with intermediate-sized spermatocytes appearing late during meiosis. PGGT-I activity was at least 10-fold lower than farnesyltransferase activity and was not significantly different among all cell populations. Differentiation-dependent in vivo protein prenylation was demonstrated by labeling of seminiferous epithelium with [3H]mevalonic acid at different prepubertal ages. Total protein prenylation and the ratio of geranylgeranylated to farnesylated protein, in contrast to prenyltransferase activity, decreased with increasing age. Although 20-30-kDa proteins were the most highly labeled at all ages, [3H]-proteins from different-aged prepubertal rats showed age-dependent changes in the level of prenylation of at least 14 proteins as determined by two-dimensional (2D) electrophoresis. Prenylated proteins of round spermatids were distinguished from those of the spermatocytes by the lack of many 20-30-kDa proteins and by low geranylgeranyl/farnesyl (GG/F) ratios. These results show that independent changes in prenyltransferase activity and protein prenylation accompany the differentiation events during the premeiotic and meiotic stages of spermatogenesis. This suggests that prenylation in the seminiferous epithelium may be more dependent on available protein substrate than on protein prenyltransferase activity.

Aging↗
PubMed2001

Determinants of variable response to statin treatment in patients with refractory familial hypercholesterolemia.

Interindividual variability in low density lipoprotein (LDL) cholesterol (LDL-C) response during treatment with statins is well documented but poorly understood. To investigate potential metabolic and genetic determinants of statin responsiveness, 19 patients with refractory heterozygous familial hypercholesterolemia were sequentially treated with placebo, atorvastatin (10 mg/d), bile acid sequestrant, and the 2 combined, each for 4 weeks. Levels of LDL-C, mevalonic acid (MVA), 7-alpha-OH-4-cholesten-3-one, and leukocyte LDL receptor and hydroxymethylglutaryl coenzyme A reductase mRNA were determined after each treatment period. Atorvastatin (10 mg/d) reduced LDL-C by an overall mean of 32.5%. Above-average responders (LDL-C -39.5%) had higher basal MVA levels (34.4+/-6.1 micromol/L) than did below-average responders (LDL-C -23.6%, P<0.02; basal MVA 26.3+/-6.1 micromol/L, P<0.01). Fewer good responders compared with the poor responders had an apolipoprotein E4 allele (3 of 11 versus 6 of 8, respectively; P<0.05). There were no baseline differences between them in 7-alpha-OH-4-cholesten-3-one, hydroxymethylglutaryl coenzyme A reductase mRNA, or LDL receptor mRNA, but the latter increased in the good responders on combination therapy (P<0.05). Severe mutations were not more common in poor than in good responders. We conclude that poor responders to statins have a low basal rate of cholesterol synthesis that may be secondary to a genetically determined increase in cholesterol absorption, possibly mediated by apolipoprotein E4. If so, statin responsiveness could be enhanced by reducing dietary cholesterol intake or inhibiting absorption.

Anticholesteremic Agents↗
PubMed1987

Synthesis of some 3-hydroxy-5-aminopentanoic acid derivatives.

The 5-amino analogues of mevalonic acid and mevalonolactone, 5-amino-3-hydroxy-3-methylpentanoic acid (VII a) and 4-hydroxy-4-methyl-2-piperidone (III a), and some related compounds were synthesized as possible inhibitors of cholesterol biosynthesis. None of them was found effective on the synthesis of cholesterol in rat liver slices and on HMG-CoA reductase activity in vitro, but 4-hydroxy-4-(4-chlorophenyl)-2-piperidone (III b) raised high density lipoproteins (HDL) in normolipaemic rats.

Amino Acids↗
PubMed2000

[Identification of the gene for hyper-IgD syndrome: a model of modern genetics].

Hyperimmunoglobulinaemia D and periodic fever syndrome (HIDS) is a rare autosomal recessive disorder. Patients suffer from recurrent attacks (3-6 days) with fever, abdominal distress, lymphadenopathy, skin lesions and arthralgias. Patients display a constantly elevated serum IgD which serves as a biological marker of the disease. Recently, the gene for HIDS was discovered by two independent groups using positional and functional cloning methods. One group used linkage analysis (positional cloning) and was able to locate the gene for HIDS on the long arm of chromosome 12 (12q24). Mevalonate kinase was an interesting candidate gene because patients with a near complete absence of this enzyme (mevalonic aciduria) do exhibit attacks of fever. Indeed subsequent data showed that there was a decreased enzyme activity due to missense mutations in the mevalonate kinase gene. The other group detected slightly elevated urinary excretion of mevalonic acid during attacks in a HIDS patient (functional cloning). The enzyme activity of mevalonate kinase was lower in cultured cells and sequence analysis identified several missense mutations in cDNA encoding for mevalonate kinase. Mevalonate kinase is a key enzyme in the cholesterol synthesis pathway and it is rather surprising that a defect in the cholesterol metabolism can cause a periodic inflammatory disease such as HIDS.

Biomarkers↗
PubMed1978

Cholesterol is a critical cellular component for T-lymphocyte cytotoxicity.

Preincubation of cytolytic T lymphocytes (CTLs) generated in secondary C57BL/6 anti-DBA/2 mixed leukocyte cultures with an inhibitor of cellular cholesterol synthesis (25-OH-cholesterol) for 24 hr strongly depressed the cytolytic activity as determined in a 3-hr 51Cr assay. The effect of the inhibitor was reversed by the simultaneous addition of cholesterol or of mevalonic acid during the preincubation period (mevalonate is the product of the regulatory enzyme in the sterol synthesis pathway, 3-hydroxy-3-methylglutaryl-CoA reductase (NADP) [mevalonate:NADP+ oxidoreductase (CoA-acylating), EC 1.1.1.34]). Because, under the same culture conditions, inhibition of DNA synthesis had no effect on CTL activity, the experiments suggest that the effect of 25-OH-cholesterol is related to its inhibitory effect on sterol synthesis, resulting in decreased levels of membrane-bound cholesterol, rather than to inhibition of cellular proliferation.

Animals↗
PubMedDate not supplied

Mevalonate kinase deficiency and Dutch type periodic fever.

Dutch type periodic fever (DPF) is an autosomal recessive hereditary fever syndrome. Cases have been reported worldwide, the majority from France and The Netherlands. From infancy the patients suffer fever attacks that recur every 2-8 weeks, often precipitated by immunizations, infections or emotional stress. Fever lasts 2-7 days and can be accompanied by malaise, headache, diarrhea, abdominal pain, vomiting, skin rashes, arthralgia, arthritis, tender lymphadenopathy, hepatosplenomegaly, and oral and genital ulcers. Laboratory evaluation during fever shows granulocytosis and elevated acute phase reactants. DPF is caused by a deficiency of the enzyme mevalonate kinase (MK). Besides DPF, the spectrum of MK deficiency includes a severe phenotype, mevalonic aciduria (MA). MA patients have less residual MK activity, leading to substantially higher urinary mevalonic acid excretion than in DPF. Mevalonic aciduria is characterized by mental retardation and dysmorphic features in addition to the clinical features of DPF. At the genomic level, several mutations of varying severity have been identified. The DPF phenotype is caused by one particular mild missense mutation. Most patients are compound heterozygotes for this mutation and a more severe mutation. The mechanism by which MK deficiency leads to fever is not understood. The vast majority of DPF patients have persistently elevated serum IgD and can be classified as having hyperimmunoglobulinemia D and periodic fever syndrome (HIDS). Conversely, most HIDS patients have MK deficiency and hence DPF, but the two disorders do not overlap entirely.

Child↗
PubMed1987

Effect of clofibrate on brain mevalonate-5-pyrophosphate decarboxylase.

The effect of clofibrate on the activity of the three mevalonate-activating enzymes has been studied for the first time in brain by reactions carried out using [2-14C] mevalonic acid as substrate and 105,000 g supernatants from 14-day-old chick brain. Mevalonate-5-pyrophosphate decarboxylase was clearly inhibited, while mevalonate kinase and mevalonate-5-phosphate kinase were not significantly affected. The effect of clofibrate on decarboxylase activity was progressive with increasing concentrations (1.25-5.00 mM) of the inhibitor. A transient inhibition and a subsequent activation as a function of clofibrate concentration seemed to occur for mevalonate kinase. Direct measurements of decarboxylase activity utilizing [2-14C] pyrophosphomevalonate as the specific substrate of this enzyme corroborated these results. Kinetic studies showed that clofibrate competes with the substrate ATP.

Animals↗
PubMed1987

Requirement for 24(S),25-epoxycholesterol for the viability of cultured fibroblasts.

Previous studies on a somatic cell mutant auxotrophic for mevalonate (Mev-1) have shown that these cells rapidly lose viability when deprived of mevalonic acid in culture medium supplemented with serum cholesterol. Testing of all known end products of mevalonate metabolism in cultured mammalian cells has been conducted to determine the basis for this mevalonate requirement. It has been found that the recently discovered mevalonate metabolite 24(S),25-epoxycholesterol produces a partial restoration of viability of Mev-1 cells starved for mevalonate, whereas other structurally similar oxysterols do not. It appears that 24(S),25-epoxycholesterol has a specific, vital cellular function in CHO-K1 cells.

Animals↗
PubMed1995

A novel type of protein modification by isoprenoid-derived materials. Diphytanylglycerylated proteins in Halobacteria.

Previous work from this laboratory has shown that a derivative of [3H]mevalonic acid is incorporated into a number of specific proteins in Halobacterium halobium and Halobacterium cutirubrum and that the major radioactive material released by treatment with methyl iodide was neither farnesyl nor geranylgeranyl compound, which have been generally accepted to be prenyl groups of a number of prenylated proteins found in eukaryotic cells, but an unknown compound (Sagami, H., Kikuchi, A., and Ogura, K. (1994) Biochem. Biophys. Res. Commun. 203, 972-978). In the current study, the unknown compound was prepared in a large amount from H. halobium cells and analyzed by reverse and normal phase high performance liquid chromatographies followed by mass spectrometry. The mass spectrum of this compound exhibited a parent ion peak (M+) at m/z 682, suggesting that it is a 1-methylthio-2,3-di-O-(3',7',11',15'-tetramethylhexadecyl)glycerol (diphytanylglyceryl methylthioether). Diphytanylglyceryl methyl thioether was chemically synthesized, and its mass fragmentation pattern was completely coincident with that of the mevalonic acid-derived material from H. halobium. These results indicate that Halobacteria contains specific proteins with a novel type of modification of a cysteine residue of the proteins with a diphytanylglyceryl group in thioether linkage.

Bacterial Proteins↗
PubMed2002

[Pharmacological and clinical properties of alendronate sodium hydrate].

Alendronate (alendronate sodium hydrate; Bonalon Tablet, 5 mg) is a nitrogen-containing bisphosphonate, which combines with the bone surface and reduces osteoclast-mediated bone resorption. It is a third-generation bisphosphonate compound, specifically distributed on the surface of bone resorption and taken into osteoclasts. Under the closed circumstances which is formed with osteoclast and the bone surface, alendronate becomes detached from the bone surface and taken into osteoclast since acid released from osteoclast leads to pH decrease (acidified). The uptaken alendronate blocks the pathway of mevalonic acid synthesis, which is cholesteric synthesis, inhibits the prenylation of GTP binding protein, and decreases the osteoclast's function by influencing the cytoskeleton. This restraint of alendronate in bone resorption against osteoclasts is reversible, showing no cytotoxicity at more than hundredfold concentration level at which action occurs. Alendronate is an agent for the treatment of osteoporosis that has established safety with regards to bone quality since it neither inhibits bone calcification nor influences fracture healing in chronic administration. The most serious morbidity in osteoporosis is developing fractures. The efficacy of alendronate on restraining fracture, as well as on increase in BMD, is evidenced in Japan. Recently, in addition to senile or postmenopausal osteoporosis, drug-induced osteoporosis, such as steroid-induced osteoporosis, has attracted attention. In this regard, alendronate has been found to be an effective agent for the treatment of osteoporosis overseas, being approved in over 90 countries and used by more than 4.5 million patients. This review will give an outline of alendronate, the preparation to have introduced a concept of Evidence Based Medicine earlier, from pharmacodynamic action to clinical efficacy.

Alendronate↗
PubMed2005

Effect of pitavastatin on transactivation of human serum paraoxonase 1 gene.

Hepatic hydroxymethyl glutary coenzyme A HMG-CoA reductase inhibitors (statins) have various anti atherosclerosis pleiotropic effects that are independent of cholesterol reduction. Human serum paraoxonase 1 (PON1) is associated with high-density lipoprotein (HDL) and inhibits the oxidative modification of low-density lipoprotein (LDL). We investigated the effects of statins on PON1 gene transcription using a reporter gene assay. Promoter activity of the PON1 gene was estimated by measuring luciferase activity of plasmids with a PON1 promoter region transfected into human hepatoma HepG2 cells and human embryonic kidney (HEK) 293 cells. Pitavastatin, simvastatin, and atorvastatin each significantly increased PON1 promoter activity, and the transactivation by pitavastatin was abrogated by mevalonic acid and farnesyl pyrophosphate (FPP), however, not by geranylgeranyl pyrophosphate. Further, PON1 promoter activity was enhanced by farnesyl transferase inhibitor (FTI), but not by geranylgeranyl transferase inhibitor (GGTI). PON1 gene transcription has been reported to be dependent on Sp1 and the transactivation by pitavastatin was completely abrogated by mithramycin, an inhibitor of Sp1. Our results suggest that pitavastatin activates transcription of the PON1 gene through the FPP pathway, which may play an important role in the anti atherosclerotic effects of statins.

Alkyl and Aryl Transferases↗
PubMed1999

New insights into the pharmacodynamic and pharmacokinetic properties of statins.

The beneficial effects of statins are assumed to result from their ability to reduce cholesterol biosynthesis. However, because mevalonic acid is the precursor not only of cholesterol, but also of many nonsteroidal isoprenoid compounds, inhibition of 3-hydroxy-3-methylglutaryl coenzyme A reductase may result in pleiotropic effects. It has been shown that several statins decrease smooth muscle cell migration and proliferation and that sera from fluvastatin-treated patients interfere with its proliferation. Cholesterol accumulation in macrophages can be inhibited by different statins, while both fluvastatin and simvastatin inhibit secretion of metalloproteinases by human monocyte-derived macrophages. The antiatherosclerotic effects of statins may be achieved by modifying hypercholesterolemia and the arterial wall environment as well. Although statins rarely have severe adverse effects, interactions with other drugs deserve attention. Simvastatin, lovastatin, cerivastatin, and atorvastatin are biotransformed in the liver primarily by cytochrome P450-3A4, and are susceptible to drug interactions when co-administered with potential inhibitors of this enzyme. Indeed, pharmacokinetic interactions (e.g., increased bioavailability), myositis, and rhabdomyolysis have been reported following concurrent use of simvastatin or lovastatin and cyclosporine A, mibefradil, or nefazodone. In contrast, fluvastatin (mainly metabolized by cytochrome P450-2C9) and pravastatin (eliminated by other metabolic routes) are less subject to this interaction. Nevertheless, a 5- to 23-fold increase in pravastatin bioavailability has been reported in the presence of cyclosporine A. In summary, statins may have direct effects on the arterial wall, which may contribute to their antiatherosclerotic actions. Furthermore, some statins may have lower adverse drug interaction potential than others, which is an important determinant of safety during long-term therapy.

Animals↗
PubMed1983

Increased deposition of cholesterol in brain after electroconvulsive seizure.

Rats injected intracranially with cholesterol precursors and subjected to electroconvulsive seizures showed significantly higher levels of deposition of [4-14C]cholesterol into brain cholesterol than controls. The degree of incorporation was cholesterol greater than mevalonic acid greater than sodium acetate; in each case convulsed animals exceeded unshocked animals. Enhanced turnover of brain cholesterol with incorporation of circulating sterol may be associated with the etiology of convulsive seizures.

Acetates↗
PubMed1994

Growth inhibition of rat liver epithelial tumor cells by monoterpenes does not involve Ras plasma membrane association.

The role of altered ras oncoprotein (Ras) farnesylation and membrane association in the growth inhibitory effects of several monoterpenes (limonene, perillic acid, perillyl alcohol, menthol, pinene and cineole) was investigated in rat liver epithelial cells. All of the above compounds except cineole inhibited the growth of viral Ha-ras-transformed rat liver epithelial cells (WB-ras cells) at concentrations of 0.25-2.5 mM. These cells, however, were not necessarily more sensitive to these compounds compared to non-transformed and viral raf-transformed rat liver epithelial cells. Growth inhibition by limonene, perillic acid and pinene was only partially restored (20-50%) by supplementing the culture medium with 2 mM mevalonic acid. Western blot analyses of cytosolic and membranous fractions of WB-ras cells treated with monoterpenes indicated no change in Ras distribution. In contrast, lovastatin, a potent inhibitor of 3-hydroxy-3-methyl-glutaryl coenzyme A reductase and Ras farnesylation, specifically reduced WB-ras cell growth and increased cytosolic levels of Ras. Thus, monoterpene-induced growth inhibition of rat liver epithelial cells was dissimilar to lovastatin and did not appear to involve altered Ras plasma membrane association.

Animals↗
PubMed1981

Stereochemistry of beta-, gamma-, and epsilon-ring formation in bacterial C50.

Cell-free systems from Corynebacterium poinsettiae and Micrococcus luteus incorporated labeled mevalonic acids into acyclic C40 and cyclic C50 carotenoids. When (3R,4R)-[2-14C,4-3H1]mevalonate was used as substrate, the 14C:3H ratios of C.p.450 and sarcinaxanthin showed that the hydrogen atoms at C-2 of both carotenoids, and that at C-6 of sarcinaxanthin, are derived from the 4-pro-R position of mevalonate. The 14C:3H ratios of C.p.450 and sarcinaxanthin synthesized from (2RS,3R)-[2-14C,2-3H2]mevalonate showed that both hydrogen atoms of C-4 are derived from those at C-2 of mevalonate. These results exclude epsilon- and beta-rings as precursors of the gamma-ring. They also exclude the interconversion of the epsilon- and beta-rings. Sarcinaxanthin samples synthesized from (3R,4R)-[2-14C,4-3H1]- and (2RS,3R)-[2-14C,2-3H2]mevalonate by a cell-free system from M. luteus were found to undergo isomerization in strong alkali. The major product of isomerization (85%) was decaprenoxanthin (epsilon-ring) with the beta-ring C.p.450 present in small amounts (3% yield). The 14C:3H ratios of these isomerization products were consistent with the loss of one C-4 hydrogen atom from each epsilon-ring of the former and one C-6 hydrogen atom from each beta-ring of the latter.

Carbon Radioisotopes↗
PubMed1992

Isoprenylation and carboxylmethylation in small GTP-binding proteins of pheochromocytoma (PC-12) cells.

1. A group of 21 to 24-kDa proteins of pheochromocytoma (PC-12) cells was found in blot overlay assays to bind specifically [alpha-32P]GTP. Binding was inhibited by GTP analogues but not by ATP. Such small GTP-binding proteins were found in the cytosolic and in the particulate fraction of the cells, but they were unevenly distributed: about 75% of the small GTP-binding proteins were localized within the particulate fraction of the cells. Separation of these proteins by two-dimensional gel electrophoresis revealed the existence of seven distinct [alpha-32P]GTP-binding proteins. 2. Targeting of the small GTP-binding proteins to the particulate fraction of PC-12 cells requires modification by isoprenoids, since depleting the cells of the isoprenoid precursor mevalonic acid (MVA) by the use of lovastatin resulted in a 50% decrease in membrane-bound small GTP-binding proteins, with a proportionate increase in the cytosolic form. This blocking effect of lovastatin was reversed by exogenously added MVA. 3. In addition, metabolic labeling of PC-12 cells with [3H]MVA revealed incorporation of [3H]MVA metabolites into the cluster of 21 to 24-kDa proteins in a form typical of isoprenoids; the label was not removed from the proteins by hydroxylamine, and labeling was enhanced in cells incubated with lovastatin. The latter effect reflects a decrease in the isotopic dilution of the exogenously added [3H]MVA, as the addition of exogenous MVA reversed the effect of lovastatin on [3H]MVA-metabolite incorporation into the 21 to 24-kDa proteins. 4. Additional experiments demonstrated that isoprenylation is required not only for membrane association of small GTP-binding proteins, but also for their further modification by a methylation enzyme. This was evident in experiments in which the cells were metabolically labeled with [methyl-3H]methionine, a methylation precursor. The group of 21 to 24-kDa proteins was labeled with a methyl-3H group in a form typical of C-terminal-cysteinyl carboxylmethyl esters. Their methylation was blocked by the methylation inhibitors methylthioadenosine (MTA), 3-deazadenosine and homocysteine thiolactone as well as by lovastatin. MVA reversed the lovastatin block of methylation. 5. Two-dimensional gel analysis of the [3H]methylated proteins detected seven methylated small GTP-binding proteins that correspond to the isoprenylated proteins. Levels of the small GTP-binding proteins as well as isoprenylation and methylation were reduced by cycloheximide. 6. Distribution of the methylated proteins between particulate and cytosolic fractions was found to be similar to that of the small GTP-binding proteins (i.e., a 4:1 ratio).(ABSTRACT TRUNCATED AT 400 WORDS)

Adrenal Gland Neoplasms↗
PubMed2003

Biogenetic studies in Syringa vulgaris L.: synthesis and bioconversion of deuterium-labeled precursors into lilac aldehydes and lilac alcohols.

Syringa vulgaris L. inflorescences were fed with aqueous solutions of regioselectively deuterated compounds assumed to be precursors of lilac aldehyde and lilac alcohol, respectively. Volatiles were extracted by stir bar sorptive extraction (SBSE) and analyzed using enantioselective multidimensional gas chromatography/mass spectrometry (enantio-MDGC/MS); deuterium-labeled lilac aldehydes and lilac alcohols were separated from unlabeled stereoisomers on a fused silica capillary column, coated with heptakis(2,3-di-O-methyl-6-O-tert-butyldimethylsilyl)-beta-cyclodextrin (DIME-beta-CD) (30%) in SE 52 (70%), as the chiral stationary phase. Feeding experiments with [5,5-(2)H(2)]mevalonic acid lactone 22 and [5,5-(2)H(2)]deoxy-d-xylose 23 indicate that the novel mevalonate independent 1-deoxy-d-xylose 5-phosphate/2C-methyl-d-erythritol 4-phosphate pathway is the dominant metabolic route for biosynthesis in lilac flowers. Additionally, bioconversion of deuterium-labeled d(5)-(R/S)-linalool 3, d(6)-(R)-linalool 21, d(5)-(R/S)-8-hydroxylinalool 6, d(5)-(R/S)-8-oxolinalool 7, d(5)-lilac aldehydes 8-11 and d(5)-lilac alcohols 12-15 into lilac during in vivo feeding experiments was investigated and the metabolic pathway is discussed. Incubation of petals with an aqueous solution of deuterated d(5)-(R/S)-linalool 3 indicates an autonomic terpene biosynthesis of lilac flavor compounds in the flower petals of lilac.

Acyclic Monoterpenes↗